Direct protection of cultured neurons from ischemia-like injury by minocycline.
10.5115/acb.2010.43.4.325
- Author:
Wendy C HUANG
1
;
Yanli QIAO
;
Lijun XU
;
Rachid KACIMI
;
Xiaoyun SUN
;
Rona G GIFFARD
;
Midori A YENARI
Author Information
1. Department of Anesthesia, Stanford University School of Medicine, Stanford, CA 94305, USA.
- Publication Type:In Vitro ; Original Article
- Keywords:
Minocycline;
Microglia;
Ischemia;
Neurons
- MeSH:
Cell Death;
Coculture Techniques;
Glucose;
Ischemia;
Matrix Metalloproteinases;
Microglia;
Minocycline;
Neurons;
Nitric Oxide Synthase Type II;
Oxygen;
Tetracycline;
Tissue Plasminogen Activator;
Tumor Necrosis Factor-alpha
- From:Anatomy & Cell Biology
2010;43(4):325-331
- CountryRepublic of Korea
- Language:English
-
Abstract:
Minocycline, a tetracycline antibiotic, is now known to protect cells via an anti-inflammatory mechanism. We further explored this effect using an in vitro model of ischemia-like injury to neurons. Coculturing neurons with microglia, the brain's resident immune cell, modestly increased cell death due to oxygen and glucose deprivation (OGD), compared to neurons alone. Treatment of cocultures with minocycline decreased cell death to a level significantly lower than that of neurons alone. Treatment of cocultures with minocycline or inhibitors of various immune mediators, also led to decreased cell death. Importantly, treatment of neuron cultures without added microglia with these same inhibitors of tissue plasminogen activator, matrix metalloproteinases, TNF-alpha and inducible nitric oxide synthase as well as minocycline also led to decreased cell death. Thus, anti-inflammatory treatments appear to be directly protective of neurons from in vitro ischemia.
